Download Chapter 13-cardiac 檔案

William J. Germann | Cindy L. Stanfield
Principles of
Human Physiology
Second Edition
14
The Cardiovascular System:
Cardiac Function
心血管系統：心臟的功能
PowerPoint® Lecture Slides Prepared by Cindy Stanfield,
University of South Alabama
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Chapter Outline 大綱
I.
Overview of the Cardiovascular System
心血管系統總覽
II.
The Path of Blood Flow Through the Heart and Vasculature
在心臟及血管系統的血流路徑
III.
Anatomy of the Heart
心臟的解剖構造
IV.
Electrical Activity of the Heart
心臟的電生理活性
V.
The Cardiac Cycle
心臟的週期
VI.
Cardiac Output and Its Control
心輸出量及其控制
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I. Overview of the Cardiovascular System
心血管系統總覽
P414
 The cardiovascular system consists of three components:

Heart 心臟—a muscular pump that drives the flow of blood through
blood vessels

Blood vessels 血管—conduits管線 through which the blood flows

Blood 血液—a fluid that circulates around the body, carrying
materials to and from the cells
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The Heart 心臟
P414-415
主動脈
上腔大靜脈
右肺動脈
左肺動脈
肺動脈幹
右肺靜脈
肺動脈
半月瓣
右心房
右房室辦；三尖瓣
右心室
左肺靜脈
左心房
主動脈半月瓣
左房室瓣
腱索
心室中隔
乳頭肌
左心室
心尖
下腔大靜脈
 The heart is a muscular organ whose function is to generate the force that propels
blood through the blood vessels
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Figure 14.1
Blood Vessels 血管
P415
Heart  Arteries  Arterioles Capillaries  Venules  Veins
•
Vasculature 血管系統 —the system of blood vessels that carry it from the heart
to the various organs and then back to the heart again  the cardiovascular
system is a closed system 密閉系統
•
Arteries 動脈 – relatively large, branching vessels that conduct blood away from
the heart
•
Arterioles 小動脈 – small branching vessels with high resistance
•
Capillaries 微血管 – site of exchange between blood and tissue
•
Venules 小靜脈 – small converging vessels
•
Veins 靜脈 – relatively large converging vessels that conduct blood to the heart
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Blood 血液
•
Erythrocytes 紅血球 – red blood cells (RBC)
–
•
Defend body against pathogens 防禦身體對抗病源菌
Platelets 血小板 – cell fragments
–
•
Transports oxygen and carbon dioxide 運送氧氣及二氧化碳
Leukocytes 白血球 – white blood cells (WBC)
–
•
P416
Important in blood clotting 對血液的凝固很重要
Plasma 血漿 – fluid and solutes
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II. The Path of Blood Flow Through the Heart and
Vasculature
在心臟及血管系統的血流路徑
•
Series Flow Through the Cardiovascular System
心血管系統的連續性流向
•
Parallel Flow Within the Systemic or Pulmonary Circuit
體循環或肺循環內的平行性流向
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Series Flow Through the Cardiovascular System
心血管系統的連續性流向
P416-417
• Pulmonary circuit 肺循環
Figure 14.2
– Supplied by right heart
– Blood vessels from heart to lungs and lungs
to heart
肺靜脈
肺動脈
• Systemic circuit 體循環
主動脈
肺循環
– Supplied by left heart
下腔大靜脈
– Blood vessels from heart to systemic
tissues and tissues to heart
左心房
•
Exchange between blood and tissue takes place in
capillaries 微血管
•
Pulmonary capillaries 肺微血管  blood entering
lungs = deoxygenated blood 去氧血  oxygen
diffuses from tissue to blood  blood leaving lungs
= oxygenated blood 含氧血
右心房
右心室
左心室
體循環
•
Systemic capillaries 體微血管  blood entering
tissues = oxygenated blood  oxygen diffuses
from blood to tissue  blood leaving tissues =
deoxygenated blood
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Parallel Flow Patterns in the Cardiovascular System
體循環或肺循環內的平行性流向
P417-419
•
Cardiovascular system = closed system 密閉系統
•
Flow through systemic and pulmonary circuits are
in series: left ventricle 左心室  aorta 主動脈 
systemic circuit 體循環  vena cavae 下腔大靜脈
 right atrium 右心房  right ventricle 右心室 
pulmonary artery 肺動脈  pulmonary circuit 肺循環
 pulmonary veins 肺靜脈  left atrium 左心房  left
ventricle 左心室
•
Aorta 主動脈  arteries 動脈  arterioles 小動脈
 capillaries 微血管 venules 小靜脈  veins 靜脈
•
Parallel flow 平行的流向 allows independent 獨立的
regulation of blood flow to organs & receives fully
oxygenated blood
•
In some exceptions, blood flows in series between two
capillary beds  hypothalamus & anterior pituitary,
intestine &liver, and kidney
•
The heart muscle obtains most of its nourishment
營養 from blood via the coronary arteries 冠狀動脈,
which branch off the aorta near its base and run
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Cummings.
Figure
14.3
through
the heart muscle
III. Anatomy of the Heart 心臟的解剖構造
•
Myocardium and the Heart Wall
心肌及心臟壁
•
Valves and Unidirectional Blood Flow
瓣膜及單方向的血流
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The Location of Heart 心臟的位置
P419-420
Figure 14.4
上腔大靜脈
主動脈
右肺
肺動脈幹
左肺
心臟
肋骨
橫膈膜
心包膜
腹腔
•
Located in thoracic cavity 胸腔 diaphragm 橫膈膜 separates abdominal cavity 腹腔
from thoracic cavity
•
Size of fist 拳頭 & weighs approximately 250 – 350 grams
•
Pericardium 心囊  membranous sac surrounding heart  lubricates 潤滑 heart
frictionInc.,
摩擦
 pericarditis
心囊炎 = inflammation of pericardium
Copyrightdecreasing
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Myocardium and the Heart Wall 心肌及心臟壁
Three layers of the heart wall:
•
Endocardium 心內膜 (inner)
 layer of endothelial cells
•
Myocardium 心肌 (middle)
 cardiac muscle
•
Epicardium 心外膜 (outer)
 external connective tissue
P420-421
Figure 14.1
 The greater thickness of the muscle of the left
ventricle 左心室 allows it to generate the force
necessary to pump blood throughout the body
 Although the entire heart muscle functions as a
unit, atrial 心房的 muscle and ventricular 心室的
muscle are physically anchored 固定to and
separated 分隔 by a layer of fibrous connective
tissue called the fibrous skeleton 纖維骨架 of the
heart
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Figure 14.5
Valves and Unidirectional Blood Flow
瓣膜及單方向的血流
P421
•
Pressure within chambers of heart vary with heartbeat cycle 心跳週期
•
Pressure difference drives blood flow 壓力差驅動血流  high pressure to
low pressure
•
Normal direction of flow: atria 心房  ventricles 心室  arteries 動脈
•
Valves 瓣膜 prevent backward flow of blood  all valves (four valves) open
passively based on pressure gradient
•
Atrioventricular (AV) valves 房室瓣  permit blood to flow from the atrium to
the ventricle
–
–
–
•
Right AV valve = tricuspid valve 三尖瓣
Left AV valve = bicuspid valve 二尖瓣 = mitral valve 憎帽瓣
Papillary muscles 乳突肌 and chordae tendinae 腱索  keep AV valves from
everting 外翻
Semilunar valves 半月瓣 (aortic valve 主動脈瓣 & pulmonary valve 肺動脈瓣)
 permit blood to leave the ventricles and enter the arteries
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Action of the AV Valves 房室瓣的作用
P422
a)
當心室鬆弛，血液進入心房，推動房室瓣尖端
向下進入心室  房室瓣打開
b)
當心室收縮，血液的壓力增加，壓迫瓣膜，
使房室瓣關閉。此時乳突肌收縮，使腱索拉緊，
避免房室瓣尖端被推進心房內。
乳突肌
(收縮)
右心房
血流方向
房室瓣膜
尖端
腱索
右心室
乳突肌
(鬆弛)
房室瓣打開
(心室鬆弛)
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房室瓣關閉
(心室收縮)
Figure 14.6
Action of the Semilunar Valves 半月瓣的作用
P423
a)
當心室收縮，血液的壓力增加，壓迫半月瓣尖端，
使半月瓣打開，允許血液流入主動脈弓及肺動脈。
b)
當心室鬆弛，進入主動脈弓及肺動脈的血液，產生
的壓力壓迫半月瓣關閉。
主動脈弓
血流方向
主動脈瓣
尖端
左心室
主動脈半月瓣打開 (心室收縮)
主動脈半月瓣關閉 (心室鬆弛)
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Figure 14.7
IV.
Electrical Activity of the Heart 心臟的電生理活性
•
The Conduction System of the Heart
心臟的傳導系統
•
Spread of Excitation Through the Heart Muscle
心肌興奮性的擴散
•
The Ionic Basis of Electrical Activity in the Heart
心臟電活性的離子變化
•
Electrical Activity in Cardiac Contractile Cells
心臟收縮性細胞的電活性
•
Recording the Electrical Activity of the Heart with an
Electrocardiogram 心電圖紀錄心臟的電活性
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The Conduction System of the Heart
心臟的傳導系統
P422
Autorhythmicity is the ability to generate own rhythm
 Cardiac muscle contractions are triggered by signals originating from
within the muscle itself  myogenic 肌源性
 The ability of the heart to generate signals that trigger its contractions on
a periodic 週期的 basis—that is, to generate its own rhythm—is called
autorhythmicity 自動性
 There are two types of autorhythmic cells:
—
Pacemaker cells 節拍器(節律點)細胞 that initiate action potentials and
establish the heart rhythm
—
Conduction fibers 傳導纖維 that transmit action potentials through the heart
in a highly coordinated manner
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Pacemaker Cells of the Myocardium 心肌的節律點細胞
肌肉細胞
Figure 14.8
P422-424
間盤
胞橋體
肌小節
細胞膜
空隙聯合的通道
間盤
電流
電流
細胞膜

Pacemaker cells are concentrated primarily in two specific regions of the myocardium: the
sinoatrial node 竇房節 (SA node) and the atrioventricular node 房室節 (AV node)

Because pacemaker cells in the SA node have a faster inherent rate of spontaneous
depolarization, and because the SA node and AV node are connected by conduction fibers, the SA
node drives the depolarization of the cells in the AV node and throughout the heart, thus
establishing the heart rate

An action potential 動作電位 generated spontaneously 自發性 in cells of the SA node spreads to
adjacent muscle cells by means of electrical current 電流 passing through gap junctions 空隙聯合
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in intercalated
間盤
Conduction Fibers of the Myocardium 心肌的傳導纖維

P423,425
Conduction fibers 傳導性纖維 are specialized to quickly conduct 快速傳導 the action
potentials generated by the pacemaker cells from place to place through the
myocardium 心肌細胞, thus triggering heart muscle contractions
•
The conduction fibers include:
–
Internodal pathways 結間路徑
–
Bundle of His 希氏束
–
Purkinje fibers 浦金氏纖維
主動脈
上腔大靜脈
竇房結
左心房
房室結
右心房
希氏束
希氏束的
左右分支
左心室
右心室
浦金氏纖維
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Figure 14.9
Spread of Excitation Between Cells 細胞間興奮性的擴散
胞橋體
P423-424
•
Atria 心房 contract first followed by ventricles 心室
•
Coordination due to presence of gap junctions and conduction
pathways
•
Intercalated disks 間盤
–
Junctions between adjacent myocardial cells 心肌細胞之間的聯合
–
Desmosomes 胞橋體 to resist mechanical stress 對抗機械性壓力
–
Gap junctions 空隙聯合 for electrical coupling 電的偶合
間盤
肌小節
空隙聯合
的通道
電流
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Figure 14.8
Initiation and Conduction of an Impulse During a Heartbeat
在心跳時脈衝的啟動及傳導

P424-425
The sequence of electrical events that normally triggers the heartbeat occurs as follows:
an action potential is initiated in the  SA node  impulses travel to the  AV node by way
of internodal pathways   bundle of His   left and right bundle branches   Purkinje
fibers  impulses travel through the rest of the myocardial cells

主動脈
上腔大靜脈
竇房結
左心房
房室結
右心房
希氏束
希氏束的
左右分支
左心室
右心室
浦金氏纖維
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Figure 14.9
The impulse is conducted to
cells of the AV node which
transmit action potentials less
rapidly than other cells of the
conduction system  delayed
by about 0.1 second (the AV
node delay)
Control of Heart Beat by Pacemakers 節律點控制心跳
P424-425
 Although the SA node and the AV node are both capable of
generating spontaneous action potentials, the heartbeat is almost
always triggered by impulses originating from the SA node
— the SA node has a higher beat frequency (70 impulses/min) than the
AV node (50 impulses/min)
— the action potential originating in the SA node travel through the AV
node  cells in the AV node go into a refractory period 不反應期
 If the SA node fails to fire an action potential or if it slows down
dramatically  the AV node will initiate action potential
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Spread of Excitation Through the Heart Muscle
興奮性在心肌的擴散
P425-426
AV node delay

It allows the wave of excitation
to spread completely through
the atria before it reaches the
ventricles
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Figure 14.10
The Ionic Basis of Electrical Activity in the Heart
心臟電活性的離子變化
快速去極化
動作電
位

Pacemaker cells can fire action
potentials in the absence of any external
stimulus, and do so in a regular, periodic
fashion  because it does not have a
steady resting potential

The slow depolarizations or “ramps” that
lead up to each action potential are
referred to as pacemaker potentials

During the initial spontaneous
depolarization (orange), PK is decreasing
and PNa is increasing  during the latter
spontaneous depolarization (yellow), PCa
is increasing and PNa is decreasing

During the rapid depolarization (green),
PCa is increasing more  during the
repolarization phase (pink), PCa is
decreasing and PK is increasing
再極化
閾值
節律點電位
(慢速去極化)
Figure 14.11
L-type Ca2+ channel open
 PCa
PK  PNa
K+ channel open
 PCa  PK
 PCa  PNa
P426-427
Copyright Funny
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Education,
publishing
Benjamin
Cummings.
channel
open Inc.,
T-type
Ca2+as
channel
open
Electrical Activity in Pacemaker Cells 節律點細胞的電活性

P428
Ion concentrations in cardiac muscle cells are similar to those in other cells—the
intracellular fluid is rich in K+ but poor in Na+ and Ca2+ compared to extracellular fluid
 thus the equilibrium potential are EK Cummings.
= -94 mV, ENa= +60 mV, and Eca = +130 mV
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Electrical Activity in Cardiac Contractile Cells
心臟收縮性細胞的電活性
P428-429
 The majority of ventricular muscle cells are unlike pacemaker cells in that they
have stable resting potentials  they also have longer-lasting action potential
(250-300 msec) with a distinctive shape that can be divided into five phase
–
–
–
–
–
Phase 0 – increased permeability to Na+
Phase 1 – decreased permeability to Na+
Phase 2 – increased permeability to Ca2+, decreased permeability to K+
Phase 3 – increased permeability to K+, decreased permeability to Ca2+
Phase 4 – resting membrane potential
去極化
再極化  PNa
Na+ channel inactivate
平原期
 PCa  PK
L-type Ca2+ channel open
再極化
 PNa
 PCa  PK
Ca2+ channel inactivate
K+ channel open
PK > Pca& PNa
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Voltage-gated
Na+ channel
open
All ion channels are
in the resting state
Figure 14.12
Electrical Activity in Cardiac Contractile Cells
心臟收縮性細胞的電活性
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P429
Table 14..2
Excitation-Contraction Coupling in Cardiac Contractile Cells
心臟收縮性細胞的興奮-收縮偶合
Figure 14.13
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P429-430
Excitation-Contraction Coupling in Cardiac Contractile Cells
心臟收縮性細胞的興奮-收縮偶合
P429-430

Cardiac muscle is excited by the spread of depolarizing current through gap junctions

The depolarization triggers the opening of Ca2+ channels in the plasma membrane and
sarcoplasmic reticulum (SR)

Calcium binds to troponin, enabling the crossbridge cycle to occur  most of the Ca2+
that binds to troponin (95%) comes from the SR, with only 5% coming from the
extracelluar fluid

To terminate contraction, Ca2+ is pumped out of the cytosol into the sarcoplasmic
reticulum and interstitial fluid  Ca2+-ATPase located in the SR &plasma membrane
and Na+-Ca2+ exchanger located in the plasma membrane
•
Properties similar to skeletal muscle
–
–
–
•
T tubules
Sarcoplasmic reticulum calcium
Troponin-tropomyosin regulation
Properties similar to smooth muscle
–
Gap junctions
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Extracellular
calcium
Recording the Electrical Activity of the Heart with an
Electrocardiogram 心電圖紀錄心臟的電性活性
P431

The electrocardiogram 心電圖 (ECG) is a noninvasive 非侵入性的 means for
monitoring the electrical activity of the heart  ECG recordings do not give
information about mechanical problems of the heart unless those problems result
from an electrical problem

Electric activity generated in nervous or muscle tissue spreads through the body
because body fluids function as conductors  the more synchronized the activity,
the larger the amplitude of signals that are recorded at a distance from the source

A Dutch physiologist, Willem Einthoven, developed the technique of ECG recordings
 the procedure is based on an imaginary equilateral triangle surrounding the heart
•
ECG is a non-invasive technique  used to test for clinical abnormalities in
conduction of electrical activity in the heart
•
Distance & amplitude of spread depends on size of potentials and synchronicity
of potentials from other cells
•
Heart electrical activity- synchronized
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Einthoven’s Triangle
Lead I: LA (+) and RA (-)
Lead II: LL (+) and RA (-)
Lead III: LL (+) and LA (-)
P431

Three electrodes 電極 are placed
are placed on limbs to form an
equilateral triangle 等三角 around
the heart

One electrode in each lead 導程 is
designated as the positive
electrode, the other as the negative

Lead I detects the potential at the
left arm (LA) minus that at the right
arm (RA)

Lead II detects the potential at the
left leg (LL) minus that at the right
arm (RA)

Lead III detects the potential at the
left leg (LL) minus that at the left
arm (LA)
Figure 14.14
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Standard ECG recording 標準的心電圖紀錄
P431-432
Figure 14.15b
•
P wave  atrial depolarization 心房去極化
•
QRS complex  ventricular depolarization 心室去極化
•
T wave  ventricular repolarization 心室再極化

Atrial reploarization is generally not detected in an ECG recording because it occurs at
the same time as the QRS complex

The phases of ECG are due to action potentials traveling through the heart muscle 
reflects patterns of action potential firing in the entire populations of heart muscle
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Standard ECG recording 標準的心電圖紀錄
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P431-432
Standard ECG recording 標準的心電圖紀錄
P431-432
The membrane potential in a ventricle contractile cell
Ventricular action
potential recorded
from a single
contractile cell in
the ventricle
ECG surface recording
of the summed electrical
activity of all cells
Figure 14.15
•
PQ segment  AV nodal delay 房室結延遲
•
QT segment  ventricular systole 心室收縮
•
TQ interval  ventricular diastole 心室舒張

The P-Q or P-R interval occurs between the onset of the P wave and the onset of the
QRS complex and is an estimate the time of conduction through the AV node

The R-R interval is the time between the peaks of two QRS complex  it represents
the time between heartbeats
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ECG Showing Various Cardiac Arrhythmias—Tachycardia & Bradycardia
心電圖紀錄不同型態的心律不整—心跳過快 & 心跳過慢
P432-433
正常

Abnormal electrical activity of heart,
called cardiac arrhythmias

Abnormal SA nodal firing can cause
either a sinus tarchycardia, which is an
abnormally fast resting heart rate (>100
beats/min), or a sinus bradycardia,
which is an abnormally slow resting
heart rate (<50 beats/min)
心跳過快 (T波反轉)
•
Sinus rhythm = rhythm generated
by SA node
•
Abnormal Heart Rates:
心跳過慢
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–
Tachycardia- fast
–
Bradycardia- slow
Figure 14.16
ECG Showing Various Cardiac Arrhythmias—Heat block
心電圖紀錄不同型態的心律不整—心阻斷

P432-433
Altered conduction through the AV can
cause various degrees of heart block:
Figure 14.16
-
During first-degree heart block,
conduction through the AV node is
slowed  causing a longer delay in
AV nodal conduction (P-Q interval)
-
During second-degree heart block,
conduction through the AV node does
not always occur  absence of QRS
complex & T wave
-
During third-degree heart block,
conduction through the AV node does
not occur at all  causing complete
dissociation of atrial and ventricular
contractions
•
1st degree block = slowed conduction through AV node  increases PQ segment & Increases
delay between atrial and ventricular contraction
•
2nd degree block  lose 1-to-1 relationship between P wave and QRS complex & between
atrial and ventricular contraction
•
3rd degree block  P wave independent of QRS complex & atrial and ventricular contractions
are independent
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
ECG Showing Various Cardiac Arrhythmias—PAC & PVC
心電圖紀錄不同型態的心律不整—早熟性心房 & 心室收縮
P432-433

Sometimes the heart is depolarized by
an electrical stimulus arising outside
the normal conduction pathway

If the depolarization occurs in an
atrium, then a premature atrial
contraction (PAC) occurs

If the depolarization occurs in an
ventricular, then a premature
ventricular contraction (PVC) occurs

PACs and PVCs are generally of little
clinical significance unless they occurs
at high frequencies
Extra contraction
•
PAC = premature atrial contraction
•
PVC = premature ventricular Contraction
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.16
ECG Showing Various Cardiac Arrhythmias—Ventricular fibrillation
P432-433
心電圖紀錄不同型態的心律不整—心室纖維顫動
Loss of coordination
of electrical activity
•
Atrial fibrillation - weakness
•
Ventricular fibrillation - death within minutes

More serious arrhythmias are fibrillation 纖維
顫動, which occur when the heart muscle no
longer has synchronized depolarization

In atrial fibrillation, atrial muscle fibers
depolarize independently, so atrial
contraction is inefficient in pumping blood to
the ventricle  weakness & lightheadedness due to decreased blood flow

Ventricular fibrillation can cause death within
minutes  the ventricles can no longer
efficiently pump the blood out to the tissues,
including the brain  ventricular muscle
cells depolarized independently

Clinicians must quickly defibrillate the
ventricular muscle to keep the person alive
 defibrillation 去纖維化 can returning
synchronous electrical activity to the heart
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.16
V.
The Cardiac Cycle 心臟週期
•
The Pump Cycle 幫浦週期
•
Atrial and Ventricular Pressure 心房及心室壓
•
Aortic Pressure 主動脈壓
•
Ventricular Volume 心室體積(容積)
•
Heart Sounds 心音
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Cardiac Cycle 心臟週期
P433
Events associated with the flow of blood through
the heart during a single complete heartbeat
1.
The various phases in the pumping action of the heart, often called the
pump cycle 幫浦週期
2.
Periods of valve 瓣膜 opening and closure
3.
Changes in atrial, ventricular, and aortic pressure 心房壓、心室壓及
主動脈壓, which reflect contraction and relaxation of the heart muscle
4.
Changes in ventricular volume 心室容積, which reflect the amount of
blood entering and leaving the ventricle during each heartbeat
5.
The two major heart sounds 心音
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Cardiac Cycle 心臟週期
P433,435
 The cycle can be divided into two major stages:
— Systole 收縮期, the period of ventricular contraction
— Diastole 舒張期, the period of ventricular relaxation
 For a heart beating at the normal resting rate of 72 beats/min
(one beat every 0.8 second)  most of the cardiac cycle (about
65%, 0.5 second) is spent in diastole, systole lasts only about
0.3 second
 This longer diastole gives the heart adequate time to fill with
blood, which is essential for efficient pumping, and it also gives
the heart muscle more time to relax, which helps prevent fatigue
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Pump Cycle 幫浦週期
P434
等容收縮期
射血期
心房收縮
等容舒張期
心室充血期
心室充血期
心室收縮期
心室舒張中-晚期
心室舒張早期
房室瓣
半月瓣

Diastole 舒張期 corresponds to phases 4 and 1, whereas systole 收縮期 corresponds to
phases 2 and 3
Figure 14.17
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Four Phases of Pump Cycle 幫浦週期的四個分期
•
Ventricular filling 心室充血期
–
–
–
–
–
•
Isovolumetric ventricular contraction 等容收縮期
–
–
–
•
Ventricle contracts  pressure increases until it exceeds atrial pressure
AV and semilunar valves closed 房室瓣及半月瓣關閉
No blood entering or exiting ventricle 沒有血液流入或流出心室
Ventricular ejection 射血期
–
–
–
•
Pressure atria > Pressure ventricles 心房壓力大於心室壓力
AV valves open 房室瓣打開
Passive phase - no atria or ventricular contraction
Active phase - atria contract
Blood moves from atria to ventricle 血液從心房流至心室
Pressure ventricles > Pressure arteries 心室壓力大於動脈壓力
Semilunar valves open 半月瓣打開
Blood moves from ventricle to aorta 血液從心室流至主動脈
Isovolumetric Ventricular Relaxation 等容舒張期
– Ventricle relaxes - decreases pressure  pressure is less than aorta
– AV and semilunar valves closed 房室瓣及半月瓣關閉
No
blood Inc.,
entering
orasexiting
Copyright © 2005 –
Pearson
Education,
publishing
Benjamin ventricle
Cummings. 沒有血液流入或流出心室
收
縮
期
(systole)
(distole)
舒
張
期
P433-435
Atrial and Ventricular Pressure 心房及心室壓
心室充血期
等容收縮期
射血期
P435-436
等容舒張期
心室充血期
房室瓣
半月瓣
Ventricle contraction
心室壓
Ventricle relaxation
心房壓
Atrial contraction
心房開始收縮


心室開始收縮
The rise in atrial pressure (pink) that occurs in late diastole (phase 1) indicates the beginning
of atrial contraction 心房收縮  this rise in pressure is small and short-lived
In middle-diastole (phase 1), the ventricular pressure (green) occurs an abrupt but small rise
 is due to atrial contraction, which adds a small volume of blood to the ventricle
Figure 14.17
 A much larger increase in pressure that corresponds to ventricular systole 心室收縮 occurs
Copyright
© 20052Pearson
Inc., publishing
Cummings.
(phase
&3) &Education,
the pressure
fallsastoBenjamin
near zero
reflect relaxation of the myocardium 心室鬆弛
Aortic Pressure 主動脈壓
P436
心室充血期




The aortic valve 主動脈瓣 opens
when ventricular pressure
exceeds aortic pressure, and
then closes when aortic pressure
exceeds ventricular pressure
The maximum pressure in the
aorta during the cardiac cycle is
the systolic pressure 收縮壓 (SP),
whereas the minimum pressure
during the cardiac cycle is the
diastolic pressure 舒張壓 (DP) 
the average pressure during the
cardiac cycle is the mean arterial
pressure 平均動脈壓 (MAP)
等容收縮期
射血期
等容舒張期
心室充血期
主動脈
半月瓣
主動脈壓
心室壓
Figure 14.19
Aortic pressure is higher than ventricular pressure during diastole 舒張期 because the aorta
主動脈 is able to store pressure (energy) during systole 收縮期  the inward force exerted
on the blood by the stretched elastic tissue in its wall
As blood leaves the aorta and the pressure falls, the wall recoils 回彈  releases the energy
 drives the flow of blood through downstream vessels during diastole even though no blood
Copyright
© 2005 ejected
Pearson Education,
Inc., publishing
Benjamin
is being
from the
heart atasthis
timeCummings.
Ventricular Volume and Stroke Volume 心室容積及心搏量
心室充血期
等容收縮期
射血期
等容舒張期
P437
心室充血期
Volume of blood in ventricle
at end of diastole
舒張末期容積
Volume of blood ejected
from heart each cycle
心搏量
心房開始收縮
The volume
does not
change


Volume of blood in ventricle
at end of systole
收縮末期容積
When the ventricle contracts (phase 3), it does not eject all of the blood contained within it
 about 60 ml of blood remains in the ventricle at the end of systole under normal resting
conditions  ESV
ESV 收縮末期容積 is determined by a number of factors, including the force of ventricular
contraction, which can be altered by autonomic neurons and hormones
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.20
Heart Sounds 心音
P437-438
Sounds occur due to turbulent flow when valves close
 The sounds of the beating heart that can be heard through a stethoscope are
called heart sounds 心音
 A soft, low-pitched “lub”, designated the first sound 第一心音, and a louder,
sharper, higher-pitched “dup”, designated the second sound 第二心音
 The first sound occur at the start of systole 收縮期 (phase 2), when the AV valves
closes 房室瓣關閉, and the second sound occur at the start of diastole 舒張期
Copyright
© 2005 Pearson
Education,
publishing as Benjamin
Cummings.
(phase
4), when
theInc.,
semilunar
valves
close 半月瓣關閉
Figure 14.21
VI. Cardiac Output and Its Control
心輸出量及其調控
•
Autonomic Input to the Heart
自律神經的訊息傳入心臟
•
Factors Affecting Cardiac Output: Changes in Heart Rate
影響心輸出量的因素：心跳速率的改變
•
Factors Affecting Cardiac Output: Changes in Stroke Volume
影響心輸出量的因素：心搏量的改變
•
Integration of Factors Affecting Cardiac Output
影響心輸出量因素的整合
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Cardiac Output 心輸出量
P438-439
 The rate at which a ventricle pumps blood is called the cardiac output (CO)
心輸出量, and it is usually expressed in liters per minute (liter/min)
 The number of contractions per minute called the heart rate (HR) 心跳速率
 the CO is determined by the HR and the volume of blood that is pumped from
each ventricle with every beat, which we known as the stroke volume (SV) 心搏量
Cardiac Output (CO) = Heart rate (HR) X Stroke Volume (SV)
 For an adult at rest, the normal resting heart rate is around 72 beats/minute and
the stroke volume is 70 ml (0.07 liter)  a normal resting CO is
CO = 72 beats/min X 0.07 liter/beat = 5 liters/min
 Regulation of the heart (or any other organ or tissue) by neural input, circulating
hormones, or any other factor originating from outside the organ is referred to as
extrinsic control 外因性控制
 When the function of an organ or tissue is regulated by factors originating from
within the organ or tissue itself, the function is said to be under intrinsic control
內因性控制
known
as autoregulation
自發性調控 or local regulation 局部調控)
Copyright
© 2005 Pearson(also
Education,
Inc., publishing
as Benjamin Cummings.
Autonomic Input to the Heart 自律神經的訊息傳入心臟
P439-440
Figure 14.22
迷走神經
(副交感神經)
竇房節
延腦
頸
椎
房室節
交感神經的
心臟神經
胸
椎

Sympathetic nerves 交感神經 travel to the SA and AV nodes as
well as to the ventricular myocardium; parasympathetic nerves
副交感神經 travel mainly to the nodes

The distribution of parasympathetic fibers is relatively sparse
稀少 in the ventricles 心室  the ventricular myocardium is
regulated primarily by the sympathetic nervous system
腰
椎
薦
椎
尾
椎
心室的心肌細胞
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
脊
交感神經鏈
Factors Affecting Cardiac Output: Changes in Heart Rate
影響心輸出量的因素：心跳速率的改變
P440-442
 A person’s heart rate depends on many factors, including his or
her age, general health, level of muscular activity, and emotional
state  the various factors involved in the minute-by-minute
regulation of heart rate 心跳速率, which is entirely under extrinsic
control
— Neural control of heart rate
 Sympathetic nerve
 Parasympathetic nerve
— Hormonal control of heart rate
— Integration of heart rate control
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Sympathetic Control of Heart Rate 交感神經調控心跳速率
P441-442

Pacemaker cells of the SA node 竇房節 receive direct input from the autonomic nervous
system  increased activity in sympathetic neurons 交感神經 to the SA node increases the
frequency of action potentials 動作電位的頻率in the pacemaker cells

Sympathetic neurons release norepinephrine (NE), which binds to b1 adrenergic receptors on
the SA nodal cells and activates the cAMP system  cAMP augments the opening of funny
channels and T-type calcium channels  the net result is an increase in the slope of
spontaneous depolarization 去極化 and a decrease in the level of repolarization 再極化

Sympathetic neurons also project to the AV node and other part of the conduction system 
 the speed of conducted &  the delay of conducted   the duration of systole 收縮期
Increase in the slope
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.23a
Figure 14.24
Parasympathetic Control of Heart Rate
副交感神經調控心跳速率
P441-442

Increased activity in parasympathetic neurons 副交感神經 to the SA node decreases the
frequency of action potentials 動作電位的頻率in the pacemaker cells

Parasympathetic neurons release acetylcholine (Ach), which binds to muscarinic
cholinergic receptors on the SA nodal cells and augments the opening of potassium
channels and suppresses the opening of funny channels and T-type calcium channels 
the net result is an decrease in the slope of spontaneous depolarization 去極化 and a
hyperpolarization 過極化 of the membrane potential

Parasympathetic neurons also project to the AV node and other part of the conduction
system   the speed of conducted &  the delay of conducted   the duration of
systole 收縮期延長
Decrease in the slope
Figure 14.23b
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.24
Hormonal Control of Heart Rate 荷爾蒙調控心跳速率
P442
 Although the function of the heart can be affected by a number of hormones,
epinephrine 腎上腺素 is significant in the minute-to-minute regulation of
cardiac function
 The effects of epinephrine , which is secreted by adrenal medulla 腎上腺髓質
in response to increased sympathetic activity, are similar to those exerted by
sympathetic activity   action potential frequency;  the velocity of
conduction   HR
 Other hormones that directly affect cardiac function include the thyroid
hormones 甲狀腺素, which are secreted by the thyroid gland, and insulin
胰島素 and glucagon 昇醣素, which are secreted by the pancreas
 These hormones primary increase the force of myocardial contraction, but
glucagon also promotes increased heart rate
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Integration of Heart Rate Control 心跳速率調控的整合
P442
 The heart rate is determined entirely by the frequency of action potential firing
by the SA node, which is in turn regulated primarily by the following:
—
activity in sympathetic neurons projecting to the SA node   HR
—
activity in parasympathetic neurons projecting to the SA node   HR
—
levels of circulating epinephrine   HR
•
SA node intrinsic firing rate = 100/min
–
•
No extrinsic control on heart, HR = 100
SA node under control of ANS & hormones
–
Rest: Parasympathetic dominates, HR = 75
–
Excitement: Sympathetic takes over, HR increases
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Affecting Cardiac Output: Changes in Stroke Volume
P443
影響心輸出量的因素：心搏量的改變
 The second important determinant of cardiac output 心輸出量 is
stroke volume 心搏量  can vary from moment to moment and
depends to several factors
— ventricular contractility 心室收縮力—a measure of the
ventricles’ capacity for generating force
 Sympathetic control
 Hormonal control
— end-diastolic volume 舒張末期容積
— afterload 後負荷—the pressure that the ventricles have to work
against as they pump blood out of the heart
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Sympathetic Nervous Control of Ventricular Contractility
交感神經調控心室的收縮力

P443-444
Ventricular contractility, like heart rate, is almost entirely regulated by the sympathetic
nervous system  as sympathetic activity increase, ventricular contractility increases,
which tends to raise cardiac output
 Action potentials trigger the release of
NE  binds to b1 receptors   cAMP
 cAMP activates protein kinases that
have four distinct effects:
— phosphorylation of L-type Ca2+
channels in the plasma membrane 
 Ca2+
— phosphorylation of Ca2+ channels in
the sarcoplasmic reticulum membrane
  Ca2+
— phosphorylation of myosin increases
the rate of myosin ATPase   the
speed of cross-bridge cycling
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.25
— phosphorylation of the Ca2+-ATPase
on the sarcoplasmic reticulum
membrane   Ca2+ reuptake 
 the rate of relaxation
Sympathetic & Hormonal Control of Ventricular Contractility
交感神經及荷爾蒙調控心室的收縮力
P443-444
 The net result is that under
sympathetic influence, contractile
cells contract faster and more strongly
 Ventricular contractility is affected by
a number of hormones, including
insulin, glucagon, and thyroid
hormones, but most importantly it is
regulated by epinephrine
Sympathetic neural activity or epinephrine:
 Like norepinephrine, epinephrine
increases myocardial contractility
 promoting increases in stroke
volume and cardiac output
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
•
increases strength of contraction
•
increases rate of contraction
•
increases rate of relaxation
Figure 14.26
The Influence of End-Diastolic Volume on Stroke Volume
舒張末期容積對心搏量的影響
P443-444
 When the rate at which blood flows into the heart from the veins (that is,
venous return 靜脈回流) changes, the heart automatically adjusts its
output to match the inflow  Starling’s low 史達林定律 of the heart  an
intrinsic control 內因性調控
 The physiological basis for the Starling effect is related to the fact that
increases in end-diastolic volume (EDV) 舒張末期容積 cause muscle fibers
in ventricular myocardium to lengthen
 Such stretching of the muscle fibers causes an increase in the force of
contraction 收縮力增加 by two mechanism:
—
cardiac muscle has an optimum length that is much greater than its resting
length and that is never reached in a healthy heart
—
stretching of muscle fibers induces an increase in the affinity of troponin for
calcium  binding between troponin and calcium   number of
crossbridges
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The Starling Curve 史達林曲線
P444-445

The Starling curve is basically a length-tension curve長度-張力的曲線 such as the one
shown in Figure 13.18 for skeletal muscle

The EDV 舒張末期容積 is measure of the length of the muscle fiber  as EDV increases,
the muscle fibers are stretched to a longer length

The stroke volume 心搏量 is a measure of cardiac muscle tension  as the force of
contraction increases, stroke volume increases

The main difference between the length-tension curve for cardiac muscle compared to
skeletal muscle is that cardiac muscle is always operating at lengths less than optimum 
thus the continuing positive slope to the curve
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 13.18
Figure 14.27
The Starling Curve 史達林曲線
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
P444-445
Family of Starling Curves 史達林曲線家族
P445

Normally, an increase in venous return 靜脈回流 causes an increase in EDV, which triggers
an increase in stroke volume according to the Starling effect

Because changes in either sympathetic activity or EDV affect the force of ventricular
contraction, but by different mechanisms

It is possible to alter stroke volume either by changing sympathetic activity without changing
EDV, or by changing EDV without changing sympathetic activity  cardiac function is
therefore described not by a single Starling curve but instead by a family of curves

In actuality, EDV and contractility can change simultaneously 同時

At any given EDV, a rise in sympathetic activity
induces an increase in the stroke volume, which is
reflected as an upward shift in the Starling curve

Under the same conditions, a decrease in sympathetic
activity induces a decrease in the stroke volume, which
is reflected as a downward shift

Upward or downward shifts in Starling curves reflect
increases or decreases, respectively, in ventricular
contractility
心室收縮力
Copyright
© 2005 Pearson
Education, Inc., publishing as Benjamin Cummings.
Figure 14.28
Significance of Starling’s Law 史達林定律的意義
P445-446
 If venous return were suddenly to increase but stroke volume did not
(assume that heart rate is constant)  with each beat, the heart would
accumulate more blood  which would eventually cause it to expand far
beyond its normal size
 Starling’s law take on a new significance  by adjusting stroke volume so
that cardiac output matches venous return, the heart regulates its size
 If a ventricle contains a large volume of blood, the muscle of the wall has
to exert greater tension to generate a given pressure  Laplace’s Law 拉
佩斯定律 (張力與容器的直徑大小及內在壓力成正比)
 Certain pathological conditions can lead to chronic enlargement of the
heart  if the ventricles get too big, they become unable to generate
enough pressure to maintain adequate cardiac output  such an inability
is called heart failure 心衰竭
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Affecting End-Diastolic Volume & Stroke Volume
影響收縮末期容積及心搏量的因素
P446-447

EDV is primarily determined by end-diastolic pressure, sometimes referred to as preload
前負荷  because it places tension (or load) on the myocardium before it begins to contract

The EDV of a ventricle is determined by the pressure of the blood inside it at the end of
diastole (preload)  as preload (end-diastole pressure) increases, EDV increases, and
stroke volume increases according to Starling’s law

Preload is determines by a number of factors
—
—
—
filling time 充血時間, which depends on heart rate
atrial pressure 心房壓, which is determined by venous return and the force of atrial contraction
central venous pressure 中央靜脈壓, the pressure of blood contained in the large veins that lead
into the heart  is affected by blood volume, muscular activity, and even changes in posture

The most important influence of venous return is central venous pressure  as central
venous pressure rises, venous return increases because the increased pressure forces more
blood to flow into the atria

Stroke volume depends not only on how much force the ventricular muscle develops, but
also on how large a force it has to work against  when the heart ejects blood, the
ventricular muscle works against arterial pressure

Because arterial pressure places a load on the myocardium after contraction starts, it is
called afterload 後負荷  increases in arterial pressure (afterload) tend to cause stroke
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
volume to decrease
Summary of Factors Influencing Stroke Volume
簡略影響心搏量的因素
P447
• End-diastolic pressure = preload 前負荷
– Filling time 充血時間
– Atrial pressure 心房壓
– Central venous pressure 中央靜脈壓
• Afterload 後負荷 = pressure in aorta during ejection

Stroke volume is influenced by three major factors:
—
ventricular contractility 心室收縮力, which is
regulated by sympathetic activity and
epinephrine
—
EDV 舒張末期容積, which is influenced
primarily by preload
—
afterlod 後負荷, which depends on arterial
pressure
Figure 14.29
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Integration of Factors Affecting Cardiac Output
影響心輸出量因素的整合
P447
 Increases in sympathetic activity are typically accompanied by decreases in
parasympathetic activity  as a result, heart rate and stroke volume tend to
increase, which raises cardiac output
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 14.30